Helida Cristina Aquino-Santos

Beyond the common comorbidities related to obesity, such as type 2 diabetes and cardiovascular diseases, impaired lung function is already known, but whether the fat distribution (sub-cutaneous, visceral) affects the lung function and pulmonary immune response are poorly known. Few evidence has shown that visceral fat is associated with insulin resistance, low-grade inflammation, and reduced lung function. In the present study, the body composition and fat distribution were evaluated by multi-frequency octopolar bioimpedance. This study demonstrated a possible association of increased visceral fat with impaired lung function in obesity grade I (n = 28; 45.46 ± 10.38 years old) women that was not observed in normal weight (n = 20; 43.20 ± 10.78 years old) and in overweight women (n = 30; 47.27 ± 10.25 years old). We also identified a negative correlation in FVC% (R² = 0.9129; p < 0.0236), FEV1% (R² = 0.1079; p < 0.0134), PEF% (R² = 0.1673; p < 0.0018), and VC IN% (R² = 0.1330; p < 0.0057) in the obesity grade I group, clearly demonstrating that higher levels of visceral fat correlate with reduced lung function, but not with sub-cutaneous fat. In addition, for the first time, a negative correlation among anti-fibrotic protein klotho (R² = 0.09298; p < 0.0897) and anti-inflammatory IL-10 (R² = 0.1653; p < 0.0487) in plasma was observed, in contrast to increased visceral fat. On the contrary, in breath condensate, a positive correlation for adiponectin (R² = 0.5665; p < 0.0120), IL1-Ra (R² = 0.2121; p < 0.0544), and IL1-Beta (R² = 0.3270; p < 0.0084) was found. Thus, increased visceral fat directly influences the impairment of lung function and the systemic and pulmonary immune response of women with obesity grade I.

Several benefits of aerobic training for asthmatic patients have been demonstrated. However, its effects on systemic inflammation and on airway remodeling mediators and lung mechanics are unknown. This prospective study included 21 intermittent and mild asthma patients, and as primary outcomes, the evaluation of pro‐ and anti‐inflammatory and pro‐ and antifibrotic mediators in exhaled breath condensate (EBC) and blood were performed, beyond the cell counting in blood and in induced sputum. Aerobic training was performed for 3 months, 3 times per week. Aerobic training increased the levels of anti‐inflammatory cytokines and of antifibrotic mediators in the breath condensate: IL‐1ra (p = 0.0488), IL‐10 (p = 0.0048), relaxin‐3 (p = 0.0019), and klotho (p < 0.0043), respectively. Similarly, in plasma, increased levels of IL‐1ra (p = 0.0147), IL‐10 (p < 0.0001), relaxin‐3 (p = 0.004), and klotho (p = 0.0023) were found. On contrary, reduced levels of proinflammatory cytokines in the breath condensate, IL‐1β (p = 0.0008), IL‐4 (p = 0.0481), IL‐5 (p < 0.0001), IL‐6 (p = 0.0032), IL‐13 (p = 0.0013), and TNF‐α (p = 0.0001) and profibrotic markers VEGF (p = 0.0017) and TSLP (p = 0.0056) were found. Similarly, in plasma, aerobic training significantly reduced the levels of proinflammatory cytokines IL‐1β (p = 0.0008), IL‐4 (p = 0.0104), IL‐5 (p = 0.0001), IL‐6 (p = 0.006), IL‐13 (p = 0.0341), and TNF‐α (p = 0.0003) and of profibrotic markers VEGF (p = 0.0009) and TSLP (p < 0.0076). Fractional exhaled nitric oxide (FeNO) was reduced after the intervention (p = 0.0313). Regarding inflammatory cells in sputum, there was a reduction in total cells (p = 0.008), eosinophils (p = 0.009), and macrophages (p = 0.020), as well as of blood eosinophils (p = 0.0203) and lymphocytes (p = 0.0198). Aerobic training positively modulates chronic airway inflammation and remodeling mediators, beyond to improve systemic inflammation in intermittent and mild asthmatic patients.